6

The Unstoppable Rise of Pesticides and Neurodegenerative Diseases

Sooner or later the risks also catch up with those who produce or profit from them.

—Ulrich Beck, Risk Society: Towards a New Modernity

“Don’t tell me that Parkinson’s disease is a disease for old people. I’ve had it since I was forty-six!” Now fifty-five years old, Gilbert Vendé is a former farm worker who participated in the Ruffec Appeal in January of 2010. With considerable difficulty speaking—a characteristic of Parkinson’s sufferers—he told his story, triggering an emotional response from the audience. In 1998, he was working as a crop manager on a large (2,500-acre) cultivation in the Champagne Berichonne region in France, when he fell victim to acute Gaucho poisoning.

Parkinson’s Disease and Gaucho: The Exemplary Case of Gilbert Vendé

Honey aficionados have undoubtedly heard about this imidacloprid-based product, manufactured by Bayer, which created “billions of victims,” to quote Fabrice Nicolino and François Veillerette—referring, of course, to indispensable pollen gatherers.¹ Launched on the French market in 1991, this so-called “systemic” insecticide is, in fact, a fearsome killer. Applied to seeds, it penetrates the plant through the sap in order to poison plant bugs that destroy beets, sunflowers, and corn, but also anything that either remotely or strongly resembles a stinging or sucking insect, including bees. It is estimated that between 1996 and 2000, some 450,000 hives quite simply disappeared in France due to the use of Gaucho and other insecticide products.2

It took the tenacity of beekeepers’ unions, who sought the court’s help, and the courageous work of two scientists—Jean-Marc Bonmatin, from the National Center for Scientific Research (Centre National de la Recherche Scientifique, CNRS), and Marc-Édouard Colin, from the National Institute of Agronomic Research (Institut national de la recherche agronomique, INRA)—to secure an opinion from the Council of State to make the French Ministry of Agriculture yield.³ The ministry would eventually ban Gaucho in 2005, despite maneuvers from some of its senior officials to fully support the product’s manufacturer. These officials included Marie Guillou, director of the very powerful Directorate-General of Nutrition (Direction générale de l’alimentation, DGAL) from 1996 to 2000 (whom we previously met in the Dominique Marchal case, when she was directing the INRA in 2005—see Chapter 4), and Catherine Geslain-Lanéelle, who succeeded her at the DGAL from 2000–2003. The latter proved her quite remarkable zeal when she refused to submit Gaucho’s marketing authorization dossier to Judge Louis Ripoll while he was searching the DGAL headquarters after an investigation had begun. In July 2006, the senior officer was nominated to the head of the European Food Safety Authority (EFSA) in Parma (Italy), where I would meet her in January 2010 (see Chapter 15).⁴

This brief historical reminder is necessary in order to understand to what extent the decisions—or nondecisions—of those who govern us have direct repercussions on the lives of the citizens they supposedly serve. As it happens, the dilatory maneuvers to keep Gaucho on the market—by denying its toxicity despite overwhelming proof—helped put some ten thousand beekeepers out of a job,⁵ and made a number of farmers, like Gilbert Vendé, sick.

Indeed, after having “inhaled an entire day’s worth of Gaucho” in October 1998, Vendé, a farm employee, suffered horrible headaches coupled with vomiting. He consulted his physician, who confirmed the poisoning; then he went back to work soon after, “as if nothing had happened.” “For years, I sprayed dozens of products,” he explained at Ruffec. “Of course, I was closed up in a cabin, but I refused to wear the gas mask, because it’s impossible to spend hours like that, you feel like you’re suffocating.” A year after his poisoning, Vendé was regularly experiencing unbearable shoulder pain: “It was so bad that I would come down off the tractor to roll on the ground,” he explained. In 2002, he decided to consult a neurologist in Tours who informed him that he had Parkinson’s disease. “I’ll never forget that appointment,” the farmer said, his voice shrouded in emotion, “because the specialist bluntly said that my disease could be due to the pesticides that I’d used.”

It is a safe bet that this neurologist was familiar with the “extensive literature suggesting that pesticide exposure may increase risk of Parkinson’s disease” as Michael Alavanja has written.6 In his 2004 systematic review, the National Cancer Institute epidemiologist cites around thirty case-control studies that show a significant statistical link between this neurodegenerative affliction and chronic exposure to “plant products” (organochlorines, carbamates, organophosphorus compounds), namely exposure to widely used molecules such as paraquat, maneb, dieldrin, and rotenone. He came to similar conclusions two years later, when he analyzed an initial set of data from the Agricultural Health Study with his colleague Aaron Blair.

Five years after their inclusion in the mega-cohort, 68 percent of participants (57,251) were interviewed. In the meantime, seventy-eight new cases of Parkinson’s disease (fifty-six pesticide users and twenty-three spouses) had been diagnosed, in addition to twenty-three cases recorded during “enrollment” (sixty users and twenty-three spouses). The results of the study show that the probability of developing Parkinson’s disease increased with the frequency of use (the number of days per year) of nine specific pesticides, the risk potentially multiplying by a factor of 2.3. In their conclusion, the authors note that “receiving pesticide-related medical care or experiencing an incident involving high personal pesticide exposure was associated with increased risk.”⁷ Reading this, I of course thought of Gilbert Vendé, since everything indicated that his acute Gaucho poisoning was an aggravating circumstance that accelerated the pathological process, initiated by chronic exposure to pesticides.

The rest of his story looks strangely like those I have already told. Faced with the refusal of the Agricultural Social Mutual Fund (Mutualité sociale agricole, MSA) to grant occupational disease status, with the justification that Parkinson’s disease is not found in the famous tables of occupational diseases, the farmer turned to the Regional Committee for the Recognition of Occupational Diseases (Comité regional de reconnaissance des maladies professionnelles, CRRMP) of Orléans, which issued an unfavorable opinion. He then took the matter to the Social Security Court (Tribunal des affaires de sécurité sociale, TASS) in Bourges, which eventually ruled in his favor in May 2006. The court based its decision on the favorable opinion given by the CRRMP of Clermont-Ferrand, which clearly performed a different reading of the available scientific literature than its counterpart in Orléans.

At the time, Gilbert Vendé was the second farmer for whom Parkinson’s was recognized as an occupational disease. Four years later, there were “a dozen,” according to the MSA’s statistics, supplied by Dr. Jean-Luc Dupupet. The Berrichon farmer then left his “home country” to live in Paris, where he now works as a volunteer at the Association France Parkinson. “Why?” he asked during the Ruffec meeting. “Simply because in our capital, I live incognito, I’m free! If I were in my countryside, they’d point at me. I wouldn’t be able to live . . .”

Toxins and Toxic Products at the Root of Parkinson’s Disease

This neurodegenerative disease, long considered an illness related to aging, was described for the first time in 1817 by Englishman James Parkinson (1755–1824) in his short An Essay on the Shaking Palsy, in which he lists its symptoms: tremors, rigid and uncontrollable gestures, difficulties in speech.8 This exceptional doctor, a geology and paleontology enthusiast, was also a political activist who used a pen name (“Old Hubert”) to write pamphlets that, in light of industrial history, today appear incredibly coherent: “Workmen might no longer be punished with imprisonment for uniting to obtain an increase of wages, whilst their masters are allowed to conspire against them with impunity,” he advised in Revolutions without Bloodshed.⁹

In his Essay on the Shaking Palsy, Dr. Parkinson does not give any explanations for the disease that would bear his name, but suggests that it has occupational or environmental origins. He was right; while the majority of cases today are declared “idiopathic”—from an unknown cause—a number of occupational and environmental factors have been identified. After World War II, researchers quite fortuitously discovered that toxins could trigger Parkinsonian symptoms, as Professor Paul Blanc reports in his book How Everyday Products Make People Sick: the researchers measured an abnormally high rate of prevalence of the disease in the aboriginal Chamorro populations on the Mariana Islands of Guam and Rota in the West Pacific.¹⁰ They put forward the hypothesis that this excess (the rate was one hundred times higher than in the United States) was due to the seeds of a small palm tree in the cycas genus, which the Chamorro would eat in the form of a flour and contains a toxin called β-methylamino-L-alanine (BMAA). Some scientists contested this explanation, arguing that the quantity of BMAA present in the flour was too low to provoke such problems. Eventually, a researcher from Hawaii ended the controversy: he observed that the aborigines were fond of bats, which frequently consume cycas seeds. Thus, BMAA would accumulate in the flying mammals’ fat, according to the process of bioconcentration (see Chapter 3). Incidentally, the extinction of bats, much appreciated for the delicacy of their flesh, would bring about a disappearance of Parkinson’s disease on the Mariana Islands.

The annals of industry confirm the role of toxic substances in the etiology of the illness. Starting in the early twentieth century, occupational physicians observed that exposure to manganese dust brought about Parkinsonian symptoms in miners or laborers working in steel mills. In 1913, nine of these cases were reported in the Journal of the American Medical Association. As Paul Blanc ironically emphasizes, the article started on an “optimistic note,” characteristic of the then budding ideology (which still lives on today) that says progress is unavoidably accompanied by “collateral damage.” “A certain indication of the humanitarian trend of modern times is the ever-increasing interest in the accidents, intoxications and diseases coincident with various trades,” the authors wrote, with the arrogance typical of those who would never have to suffer from the evils they bent over backward to minimize.¹¹

Over the course of the twentieth century, scientific studies started to pile up throughout the world on the psychiatric effects produced by exposure to metals (notably in welding workshops), including “manganese madness,” which manifests itself by hallucinations and uncoordinated gestures, considered precursor symptoms to Parkinson’s disease. In 1924, a study carried out on monkeys allowed for the understanding of manganese’s effect on the central nervous system: it causes the premature death of certain neurons, and the loss in turn causes a decrease in the production of dopamine, a neurotransmitter necessary for the control of motor functions.¹²

Until the 1980s, scientific literature only covered nonorganic forms of manganese—in other words, simple oxides or metal salts used in industrial applications. But in 1988, a study published in the journal Neurology revealed that farm workers tasked with spraying maneb, a manganese-based fungicide, developed early signs of the Parkinson’s disease.¹³ These results were confirmed by another study published six years later, concerning a thirty-six-year-old man who had used maneb on his barley seeds for two years before developing the disease.¹⁴ Similar effects were observed in those using mancozeb, a similar fungicide still used today, as is maneb.

Finally, the role of toxins in the onset of the illness was confirmed by a series of observations carried out on drug addicts in California. In 1980, doctors noted that the injection of synthetic heroin, called “MPPP,” triggered the disease. MPPP contains a contaminant, MPTP, a derivative of which—cyperquat—is structurally similar to the widely used herbicides paraquat and diquat. The “MPTP model,” which facilitates comprehension of biological mechanisms leading to Parkinson’s disease, has been the subject of multiple studies on monkeys.15 It has been used notably to test the effects of rotenone, a natural toxin produced by certain tropical plants and present in the composition of numerous insecticides. Researchers have observed that when injected in repeated small doses, rotenone induces Parkinsonian symptoms in rats.¹⁶

Again, it should be noted that, like methyl bromide, rotenone was prohibited by the European Commission in 2009, but France obtained a special dispensation to use it on apples, peaches, cherries, grapevines, and potatoes until October 2011.¹⁷ Following Rachel Carson’s example in Silent Spring, it is now more important than ever to find an answer to the question, “Who makes this kind of decision?” Who decides that the agronomic advantages of a poison outweigh the health considerations and risks faced by those who handle them, but also, as we will see, by consumers? All the more when we can easily imagine the number of patients and deaths that had to accumulate in experimental laboratories and morgues before the European institution finally decided to act. That France systematically requests a “grace period”—to borrow the expression used by the French newspaper Le Syndicat agricole (The Agriculture Union) used in 2007 in relation to the prohibition of Monsanto’s Lasso—is, quite simply, scandalous.¹⁸

A Disease of the Industrial World

“In view of the fundamental similarities between the vertebrate and invertebrate nervous systems, insecticides designed to attack the insect nervous system (organochlorines, pyrethroids, organophosphoruses, and carbamates) are clearly capable of acute and long-term neurotoxic effects in humans,” the World Health Organization (WHO) writes in its prevention manual published in 2006 (see Chapter 3). The venerable institution specifies: “Symptoms may appear immediately after exposure or be delayed. They may include limb weakness or numbness; loss of memory, vision or intellect; headaches; cognitive and behavioral problems; and sexual dysfunction.”¹⁹

Everything the WHO describes, with the clinical coldness so characteristic of “experts,” has been observed in numerous epidemiological studies, which are impossible to present in their entirety. They concern Parkinson’s and Alzheimer’s diseases, which affect 800,000 people in France, with 165,000 new cases every year, and amyotrophic lateral sclerosis, also called “Lou Gehrig’s disease.” Isabelle Baldi, an epidemiologist, demonstrated in a study published in 2001 that exposure to a number of pesticides used on grapevines brought about a reduction in cognitive function (selective attention, memory, speech, ability to process abstract information) in winemakers in the Bordelais region. The investigation, named “Phytoner,” dealt with 917 farmers affiliated with the MSA: 528 had been directly exposed to pesticides for at least twenty-two years; 173 had been exposed in an indirect way through contact with leaves or grapes treated with them; and 216 had never been exposed (control group). After being submitted to mental aptitude tests, the subjects directly exposed were three times more likely to respond erroneously to the questions they were asked. Another very troubling fact: the subjects exposed to pesticides in an indirect way answered almost as poorly as those directly exposed.20

This reminds me of the fate of the students at the Bonne-Terre high school in Pézanas, destined to join the family winemaking business, where they would be in contact with a multitude of poisons. In another study published in 2003, Isabelle Baldi and Pierre Lebailly showed that exposure to pesticides, used namely in the vineyards of Gironde, raised the risk of developing Parkinson’s disease by a factor of 5.6 and Alzheimer’s by 2.4. These results were the product of a prospective study (named “Paquid”), where 1,507 people over the age of sixty-five were followed for ten years.²¹

“What is regrettable,” explained Caroline Tanner, neurologist at the Parkinson’s Institute in Sunnyvale, California, where I met her on December 11, 2009, “is that all the data we’ve accumulated on human populations was already obtained on lab animals decades ago.”

“You mean that the results of experimental studies can be extrapolated to humans and that they should be used to take action, for example by taking suspect products off the market?” I asked.

“Exactly! The ideal would even be that the products are tested before they go on the market to avoid painful human tragedies,” the scientist answered without hesitation, employing the straightforwardness only found on that side of the Atlantic.

The author of numerous publications on Parkinson’s disease, Caroline Tanner is one of the most renowned neurologists in the United States. She works in a “privileged place,” since the Parkinson’s Institute is “simultaneously a care and research center.” In association with the interpretation of data gathered by the Agricultural Health Study, in 2009 she published a case-control study showing that exposure to pesticides significantly raised the risk of developing Parkinsonian symptoms.²²

“We observed that the risk could be multiplied by a factor of three after exposure to three pesticides: 2,4-D and paraquat, two herbicides, and permethrin, which is an insecticide,” she commented. “Our work came at just the right time for Vietnam veterans who were exposed to Agent Orange, which includes 2,4-D in its makeup. They had requested that Parkinson’s disease be added to the list of diseases giving the right to compensation and medical care by the Department of Veterans Affairs, which they eventually obtained.23 We were surprised about paraquat, because the Parkinson’s Institute has worked a lot on MPTP,²⁴ and they are two very similar molecules. Finally, our results are worrying for permethrin, because it is an insecticide widely used in the prevention of malaria. It is found soaked into mosquito nets, military uniforms, or even basic clothing, and a lot of people can come into contact with it through the skin.”

“Is exposure time an important factor?”

“According to our study, it isn’t a determining factor. Incidentally, one of the surprises was that the wives of farmers also presented a higher risk than the general population. In reality, they are also exposed to the products, because they sometimes take part in the preparation of the fungicides, but also because they wash their husband’s clothes, or simply because they live in a polluted environment or consume contaminated food. I took part in a study with some colleagues in Honolulu, who compared male twins where one of them had developed Parkinson’s and the other hadn’t. We observed that one of the risk factors was the consumption of dairy products. The hypothesis we put forward was that persistent organic pollutants, the notorious ‘POPs,’ some of which have neurotoxic effects, like dioxins or PCBs [polychlorinated biphenyls], have the ability to accumulate in milk fat. It would be interesting to conduct a study specifically on the subject, even more so because a recent experiment showed that the combination of paraquat and maneb, a manganese-based herbicide, considerably raised the risk of Parkinson’s disease and could induce symptoms of the disease in animals that had been exposed in utero.”

“They often say that Parkinson’s disease is on a clear rise in industrialized countries, is that true?”

“Actually, we don’t know! For a very simple reason, which is that we don’t have records old enough to be able to confirm it with any certainty. I asked that question myself, and to answer it, I went to China about twenty years ago, at a time when the process of agricultural industrialization wasn’t advanced and when Parkinson’s disease was very rare. I directed a number of research projects there, and I can say that today the illness has become as common there as in the United States. The only explanation is that in twenty years, the country has been greatly industrialized, and ever since then they have been using the same pesticides as in Western countries.”

Pesticides Widely Miss Their Target, but Don’t Spare Mankind

A few days later, on January 6, 2010, I went to La Pitié-Salpêtrière hospital in Paris to meet Dr. Alexis Elbaz, a neuroepidemiologist who works for a unit at the National Institute of Health and Medical Research (Institut National de la Santé et de la Recherche Médicale, INSERM). This young researcher is a pioneer in France, one to whom Gilbert Vendé is deeply indebted. It was while reading an article in Le Quotidien du médecin (Physician’s Daily) in 2004 that Maître Gilbert Couderc, the Berrichon farm worker’s attorney, discovered that one of Dr. Elbaz’s studies, which showed a positive correlation between exposure to pesticides and Parkinson’s disease, had just won the Prix Épidaure.25 “We felt reassured,” Gilbert Couderc said. He hurried to share the invaluable publication with the CRRMP.²⁶

At the time of our interview, Alexis Elbaz had just published a new study in Annals of Neurology that he had conducted in close collaboration with the MSA—further proof, if it was needed, that the mutual fund had indeed decided to shed light on the health consequences of pesticide use.²⁷ In this case-control investigation, 224 farmers with Parkinsonian symptoms were compared to a group of 557 healthy farmers, all originally from the same region and affiliated with the MSA.

“The occupational medicine specialists at the MSA played an integral role,” the neuroepidemiologist explained. “They went to farmers’ homes and meticulously pieced together with them their exposure to pesticides over their entire professional life. They gathered a large amount of information, such as the surface area of cultivations, the type of crops and the pesticides used, the number of years and annual frequency of exposure, and the method of spreading—with a tractor or with the aid of a backpack reservoir. They carried out true detective work, taking into account all the documents the farmers supplied: farm bureau or farming co-op recommendations, which are usually strictly followed; treatment calendars; invoices; empty containers that might have been kept on the farm. All these data were then evaluated by experts, who checked their validity.”

“What was the result?”

“We observed that organochlorine insecticides raised the risk of Parkinson’s disease by a factor of 2.4. Among those are DDT and lindane, which were widely used in France between 1950 and 1990. One of their characteristics is that they remain in the environment several years after use.”

“Do you know if pesticides used in the fields can also affect residents living close to the treated areas?”

“We don’t have any data on that subject, but it’s true that, beyond exposure at elevated levels in a professional context, our results raise the question of consequences of exposure at weaker doses, such as that observed in the environment—in other words, in the water, in the air, and in food. To date, only one study has been able to provide a convincing answer.”

Published in April of 2009, the study to which Dr. Elbaz referred was conducted by a team of researchers from the University of California in the Central Valley of California.28 The researchers had a precious advantage, one that France unfortunately cannot claim. Since the 1970s, the richest state in America has required that all pesticide sales, including the indication of their planned place and time of use, be recorded in a centralized computer system, called the Pesticide Use Reporting (PUR) database. This makes it possible to know, down to the day, which geographical sectors were treated and with what chemicals; this was how Sadie Costello’s team was able to “reconstruct the history of agricultural pesticide exposure in the residential environment” of the entire region under study, between 1975 and 1999. To do this, the study participants—368 with Parkinsonian symptoms and 341 without (control), all living in California’s Central Valley—provided their addresses so their exposure level over the course of the twenty-four-year period could be calculated.

Before finding out the very troubling results of this remarkable work, it would be useful to understand its relevance, as it concerns all of us. Indeed, as David Pimentel, an American professor at the College of Agriculture and Life Sciences at Cornell, explained in 1995, “Less than 0.1 percent of pesticides applied for pest control reach their target pests. Thus, more than 99.9 percent of pesticides used move into the environment where they adversely affect public health and beneficial biota, and contaminate soil, water, and the atmosphere of the ecosystem.”²⁹ Some observers are slightly less pessimistic, like Hayo van der Werf, an agronomist at the INRA: “Each year an estimated 2.5 million tons of pesticides are applied to agricultural crops worldwide,” he wrote in 1996. “The amount of pesticide coming in direct contact with or consumed by target pests is an extremely small percentage of the amount applied. In most studies the proportion of pesticides applied reaching the target pest has been found to be less than 0.3%, so 99.7% went ‘somewhere else’ in the environment.”30 And, he adds, “Since the use of pesticides in agriculture inevitably leads to exposure of non-target organisms (including humans), undesirable side-effects may occur on some species, communities, or on ecosystems as a whole.”

As we will see, chemical agriculture is anything but an exact science, to the point that we end up wondering how and in the name of what we could have allowed the establishment of such a system of generalized poisoning on our land: “The pesticides which reach the soil or plant material in the target area begin to disappear by degradation or dispersion,” van der Werf continues. “Pesticides may volatilize into the air runoff or leach into surface water and groundwater, be taken up by plants or soil organisms or stay in the soil. The total seasonal losses in runoff for soil-surface applied pesticides average about 2% of the application and rarely exceed 5–10% of the total applied; the fraction removed by leaching is generally less. In contrast, volatilization losses of 80–90% have sometimes been measured within a few days after application. [ . . . ] Worries about the movement of pesticides in the atmosphere have arisen during the 1970s and 1980s. Transport and redeposition of pesticides may occur over very long distances, as evidenced by the presence of pesticides in ocean fog and arctic snow.”³¹

After reading about such a catastrophic scenario, it’s hard not to wonder: Does this at least do something? Have the “pests” all been exterminated? No! That’s what Professor David Pimentel explained as early as 1995: “Worldwide, an estimated 67,000 different pest species attack agricultural crops. Included are approximately 9,000 species of insects and mites, 50,000 species of plant pathogens, and 8,000 weeds. In general, less than 5% are considered serious pests. [ . . . ] Despite the yearly application of an estimated 2.5 million tons of pesticides worldwide, plus the use of biological controls and other non-chemical controls, about 35% of all agricultural crop production is lost to pests. Insect pests cause an estimated 13% crop loss, plant pathogens 12%, and weeds 10%.”³²

To sum up: the poisons poured onto fields generally miss their targets—either because pests resist or escape them, or because they “go somewhere else,” to use Hayo van der Werf’s expression—and contaminate the environment. Hence the extremely relevant question posed by Sadie Costello’s team: Can pesticides induce Parkinson’s disease in people living in proximity to treated crops? The answer is clearly affirmative. Pesticide use records have indicated that maneb, the manganese-based fungicide I have already mentioned, and the inescapable paraquat are both included among the most widely used products in California’s Central Valley. The study’s results showed that living less than five hundred yards from a treated area increased the risk of developing the disease by 75 percent. What’s more, the probability of onset of the illness before the age of sixty was multiplied by two if there was exposure to one of the two pesticides (OR: 2.27) and by more than four (OR: 4.17) if there was combined exposure, especially if the exposure took place between 1974 and 1989, that is to say when the people in question were children or teenagers.

Beate Ritz, professor of epidemiology at the UCLA School of Public Health, who supervised the University of California team’s work, explained that “the new study confirms previous observations in animal studies.” First, “exposure to multiple chemicals may increase the effects of each chemical,” which is important, because humans are generally exposed to more than one pesticide in the environment. Secondly, “the timing of the exposure is an important risk factor.”33

Pesticides and Immunotoxicity: Affecting Whales, Dolphins, and Seals

In a 1996 report entitled Pesticides and the Immune System: The Public Health Risks, which was commissioned by the prestigious World Resources Institute (WRI) in Washington, DC, Robert Repetto and Sanjay Baliga write: “The scientific evidence suggesting that many pesticides damage the immune system is impressive. Animal studies have found that pesticides alter the immune system’s normal structure, disturb immune responses, and reduce animals’ resistance to antigens and infectious agents. There is convincing direct and indirect evidence that these findings carry over to human populations exposed to pesticides.”³⁴

“That document sparked the chemical industry’s wrath,” explained Robert Repetto, an economist who specializes in sustainable development and who was vice president of the WRI when the report was written. “It was the first time a study had gathered all the available data on the effects of pesticides on the immune system, a subject that was completely underestimated at the time and, in my opinion, continues to be now, even though it is crucial to understanding the epidemic of cancer and autoimmune diseases that are observed, notably in industrialized countries.”³⁵

Indeed it is—and we will revisit this—as cancer is rarely caused by one factor alone; more often it is the result of a complex and multifactorial process, generally initiated by the action of pathogens (or of antigens), such as rays, viruses, bacteria, toxins, or chemical pollutants, and possibly favored by genetic predispositions, lifestyle, or diet. In good health, the body can defend itself against the aggression of pathogens by mobilizing its immune system, whose function is precisely to track and eliminate intruders using the action of three distinct, but complementary, mechanisms.

The first, which biologists call “nonspecific immunity,” involves macrophages and neutrophils that consume invaders (the process is called “phagocytosis”), and natural killer (NK) lymphocytes, whose mission is to exterminate them. The second, named “humoral immunity,” activates B lymphocytes, producing antibodies. Finally, the third, “cellular immunity,” sets T lymphocytes (T4 or T8) in motion, which poison the intruders that were phagocytized by the macrophages thanks to the secretion of lymphotoxins.

In their lengthy report, Robert Repetto and Sanjay Baliga devote fifteen pages or so to the numerous in vivo (that is, directly on animals) or in vitro (on cell cultures) studies that have shown that pesticides can disturb one or more of the mechanisms that make up the immune system.36 From this long list, of which organochlorines (DDT, lindane, endosulfan, dieldrin, and chlordecone) make up the lion’s share, I chose the example of atrazine, an herbicide that was banned in Europe in 2004 but continues to be used in massive quantities, notably in the United States (see Chapter 19). When administered orally to mice, atrazine disturbs the action of T lymphocytes as well as the process of phagocytosis by macrophages.³⁷ In another study published in 1983, researchers demonstrated an effect on the weight of the thymus in exposed rats. (The thymus is an essential organ in the immune system, as it is where T lymphocyte maturation takes place, and it also plays a role in the protection against autoimmunity³⁸—that is, the fabrication of antibodies, which, instead of attacking intruders, target immune system cells. Finally, another experiment in 1975 revealed that salmon exposed to atrazine through oral or cutaneous methods showed a lower weight of the spleen, an organ involved in controlling bacterial infections, such as pneumococcal or meningococcal ones.³⁹

However, as Repetto and Baliga point out, the immune system anomalies observed in lab animals following exposure to pesticides have also been observed in wild fauna. For example, in Canada, autopsies of whales found dead on the shores of the St. Lawrence Estuary showed an elevated concentration of organochlorine pesticides and PCBs, as well as an abnormal rate of bacterial infections and cancer. Sylvain de Guise, who conducted a study on the abnormally high death rate of the cetaceans, explains that only “two factors could have contributed to such a high prevalence of neoplasms in that single population: exposure to carcinogenic compounds and decreased resistance to the development of tumors.”40

Similarly, in the early 1990s, a strange epidemic decimated the dolphins of the Mediterranean; dozens of their corpses turned up on the coast of Valencia, in Spain. Autopsies revealed that the marine mammals had succumbed to an infection brought on by viruses they could normally overcome (such as morbillivirus). “We have gone back over the literature for more than a hundred years and we have found nothing like it, no other cluster of virulent epidemics like we have now,” a British researcher commented.⁴¹ In the end, studies concluded that the mass deaths had to be due to lowered immune defenses in the dolphins, whose bodies had accumulated organochlorine pesticides, PCBs, and various chemical pollutants in their bodies.⁴²

The studies conducted on fauna showing the immunosuppressive effects of pesticides are numerous, but one of them is particularly impressive. It all started during the 1980s, when zoologists noticed that seals living close to ports in the Baltic and North Seas were succumbing in huge numbers to morbillivirus infections. Dutch researchers decided to conduct a prospective experiment. They captured baby seals off the northwest coast of Scotland, considered relatively unpolluted. The friendly mammals were divided into two groups: the first was fed with herring from the Baltic Sea, where the pollution rate is significant; the second was fed with herring caught in Iceland, where contamination is very low. It is worth noting that the herring for both groups was bought at “normal” markets—that is, destined for human consumption. After two years, the fat of the seals in the first group showed a concentration rate of organochlorine pesticides ten times higher than that of the control group. The researchers also observed that the seals fed with contaminated herring had immune defenses three times weaker than those of the control group, notably with a very clear reduction in NK cells and T lymphocytes, and lower neutrophil levels and antibody responses.

At a conference held in February 1995 in Racine, Wisconsin, where he presented his team’s work, Dutch virologist Albert Osterhaus noted that this was “the first demonstration of immunosuppression in mammals as a result of exposure to environmental contaminants at ambient levels found in the environment.”⁴³ Incidentally, it’s worth noting the title of the conference: “Chemically-induced Alterations in the Developing Immune System: The Wildlife/Human Connection.”

Allergies and Autoimmune Diseases: Effects on Humans

As Robert Repetto and Sanjay Baliga point out, “the immune systems of all mammals (but also of birds and fish) have similar structures,” and what happens to whales, dolphins, or seals concerns us directly. They cite as evidence studies carried out on cyclosporine, an immunosuppressant medication prescribed to organ transplant recipients to stop the body from rejecting the transplant. Researchers observed that the drug “has been found to have similar toxicological and immunosuppressive properties in a wide variety of mammalian species, including rats, mice, monkeys and humans,” which, in the long run, lay the grounds for cancer. Indeed, as shown by Arthur Holleb, an oncologist and former chief medical officer of the American Cancer Society, patients treated with cyclosporine are one hundred times more likely to develop lymphatic cancer, in particular leukemia and lymphoma.44 Need we recall that these are precisely the malignant tumors for which farmers show a heightened risk?

In their report, Repetto and Baliga present several studies carried out by Soviet scientists, who scrupulously took a census of the effects of pesticides on the immune system. “It was very valuable, because at the time, Western studies were only interested in cancer and neurodegenerative diseases,” Repetto explained during our phone interview. “Also, the communist bureaucracy was an advantage: as there was no profit mentality—which is different from capitalist countries, where manufacturers are interested in hiding the toxicity of their products, out of fear of seeing their sales drop—the Soviet researchers carried out what was essentially true health monitoring, by conscientiously recording all the effects observed in farming populations, with the goal of lowering the health care costs they might generate.”

At the risk of seeming like an inveterate crypto-communist, I must admit that listening to these words, I thought that there was some merit to the “bureaucratic” scientific research—meaning independent from private interests—and that this outdated model should inspire regulatory agencies that generally forget to include potential medium- or long-term health care costs in their evaluation of chemical products. People will retort that the studies by “bureaucratic” researchers have not prevented catastrophic pollution of vast areas of the former Soviet Union (such as the Aral Sea), which is true. Nevertheless, as we will see later on, the explosion of chronic illnesses is tugging strongly at the purse strings of social security systems, which fall prey to a regulatory system where agro-economic considerations (the famous “benefits” pesticides supposedly offer) take precedence over health considerations (the “risks” associated with said “benefits”).

In the meantime, the “bureaucratic” scientific literature has nonetheless shown that exposure to pesticides causes autoimmune reactions; it also leads to a disturbance in neutrophil and T lymphocyte activity, which contributes to the development of pulmonary and respiratory infections. Several studies conducted between 1984 and 1995 in the cotton-producing regions of Uzbekistan, where large quantities of organochlorine and organophosphorus insecticides were sprayed, showed extremely elevated rates of respiratory, gastrointestinal, and kidney infections not just in farm laborers, but also in the populations living close to the treated zones. At the same time, in the West, researchers were showing that exposure to pesticides such as atrazine, parathion, maneb, and dichlorvos triggered allergies, leading to what Dr. Jean-Luc Dupupet calls “cutaneous manifestations” (see Chapter 3), or in other words, types of dermatitis that are the expression of an immune system reaction to a chemical aggression.⁴⁵

In its manual for pesticide poisoning prevention published in 2006, the WHO devotes a significant portion to autoimmune diseases and allergies, the prevalence of which keeps rising, especially in children.⁴⁶ The manual notes: “Allergies can have many manifestations, including hay fever, asthma, rheumatoid arthritis and contact dermatitis. The cause of allergies is a hypersensitivity response which occurs after exposure to some occupational and environmental agents. Antigens that cause allergic responses are called ‘allergens.’ [ . . . ] When the immune system loses the ability to distinguish between the body’s own cells and foreign cells, it attacks and kills host cells, resulting in serious tissue damage. This condition is called ‘autoimmunity’. Although it is not as common as immunosuppression or allergy, occupational exposure to certain chemicals has been associated with autoimmune responses.”⁴⁷

During our phone interview, Robert Repetto said that the report he wrote for the WRI triggered a lively (allergic!) reaction from manufacturers, whose scientists, just this once, decided to collectively author a “critique” in the journal Environmental Health Perspectives.⁴⁸ The selection’s signatories included licensed epidemiologists from Dow Chemical (Carol Burns and Michael Holsapple), Zeneca (Ian Kimber), DuPont de Nemours (Gregory Ladics and Scott Loveless), BASF (Abraham Tobia) and, of course, Monsanto, meaning Dennis Flaherty and John Acquavella, the author of the controversial meta-analysis I discussed in Chapter 5. After offering a firm criticism of the report, notably of the Soviet studies that they deemed “difficult to evaluate,” the authors end their article with remarks that are contradictory, to say the least. It is unclear whether they express embarrassment or a well-calculated conciliatory strategy. They write that they “do not find consistent, credible evidence” that there is a widespread phenomenon of immunosuppression linked to pesticide exposure. Nonetheless, the WRI report is an important document because it focuses attention on a potentially important issue for future research and brings a substantial literature of foreign language studies to the attention of Western scientists.

Here we have a perfect example of “the art of blowing hot and cold.” But, as we will see, when it comes to neutralizing the impact of studies not in their favor, manufacturers’ attitudes can be much more drastic, even perverse. But before examining how the regulation of chemical products that come into contact with the food chain functions, it is important to go back to the industrial history of the twentieth century, in order to understand how extremely toxic compounds managed to poison the environment and human populations, not just in the short term, but for many years to come.